According to the National Institute on Drug Abuse (NIDA), in 1997 about 1. 5 million Americans were current cocaine users (had used cocaine in the month before the survey). Because of underreporting, the Office of National Drug Control Policy estimated that the true figure was closer to 3. 6 million. Although these numbers represent a significant decrease from the 5. 7 million reported in 1985, they indicate that cocaine remains an important drug of abuse (Karen et al. 1998).
Cocaine or crack (the smoked form of the drug) affects areas of the deep brain, including the ventral tegmental area (VTA) and the nucleus accumbens, one of the brain’s main pleasure centers. During a pleasurable event, neurons originating in the VTA release the neurotransmitter dopamine into the nucleus accumbens to stimulate reward pathways. After dopamine acts, transporter molecules carry it back into the transmitting neuron. Cocaine works, at least in part, by binding to the transporter molecule and preventing the reuptake (re-absorption) of dopamine.
As dopamine accumulates in the synapse (the space between neurons), cocaine abusers experience the resulting stimulation as euphoria. But eventually the brain becomes tolerant to dopamine, and larger or more frequent doses are needed to achieve the same effect. Drug abuse may also result from stress, and in at least one study, craving for cocaine was reduced by a compound that blocks the action of corticotropin releasing factor (CRF), a hormone that initiates the stress response.
Other research involves CART peptides, natural brain substances that have some of the same effects as cocaine and may be the body’s own version of the drug, just as endorphins are the body’s opiate equivalents (Brian et al. 1994). Psychological Effects of Cocaine Acute panic-anxiety reaction, which may manifest itself in feelings of paranoia, acute anxiety, fear of insanity, and fear of impending death, is the most common adverse reaction among American users. These effects are more likely to occur in novice users or after surreptitious administration.
If cocaine is socially acceptable anxiety reactions constitute about 1 percent of all responses, however, in settings in which the drug represents a greater degree of social deviance, as many as 25 percent of first-time users panic. Although the acute-panic reaction is the most common acute, adverse reaction noted in the United States, there have been reports from Eastern countries of cocaine psychosis, however, most admission to psychiatric institutions in these countries made by police.
Cocaine is the easiest and least complicated reason police to use (Peter ; O’Leary, 1999). There are several psychological effects of taking cocaine. Some of the are given below: Anxiety Several researchers have communicated with people who had been involved in taking cocaine and it is commonly found that anxiety is the leading psychological effect of cocaine rather than depression. This has been confirmed by several published clinical reports. There is a possibility that cocaine attacks the serotonergic terminals that are responsible for controlling anxiety.
Thus it is said that cocaine causes impairment of the psychic defenses and thus affecting anxiety generating material (Alan 1996). Depersonalization Depersonalization means the feeling when one does not feel any emotion and feel detached and unreal. This type of feeling is quite unpleasant. A glass wall seems to come between the sufferers and world (Crits-Christoph 1999). Derealization This type of feeling results when one feels that the environment is not real and thus usual emotional components are avoided.
The feelings of depersonalization and derealization are also found in other mental disorders such as anxiety, depression, temporal lobe epilepsy and schizophrenia (Crits-Christoph 1999). Depression When people take cocaine, they undergo through different moods. The most common among them is low mood in which the person feels the ‘come-down’. People used to take cocaine usually come out of this feeling by using other drugs. A longer lasting depression is also resulted from the chronic use of cocaine (Gawin & Ellinwood 1988) Cognitive Shortfalls
It is quite difficult to perform a research to find out the cognitive deficits that are caused by the use of cocaine. A large number of variables responsible for the situation are there (Gawin & Ellinwood 1988). The Pandora’s Box Syndrome When people take a large quantity of cocaine for a long period, there mental state changes to internal, mental imagery that is of very high level. They do not undergo any perceptual disorder. This can be explained as if the defenses that separate the conscious from the unconscious get perforated thus allowing the percolation of material through the conscious.
This condition can not be regarded as a serious condition. The person affected can easily go to work or other life businesses. In such syndrome, impairment of attention and concentration takes place that results in a temporarily poor memory as the mind is not ready to give attention to the new information. Thus it can be said that the person has lack of focus (Gawin & Ellinwood 1988). Flashbacks The cocaine users have described flashbacks. People experience flashbacks due to traumatic drug experiences.
So it can be suggested that flashback are a form of post-traumatic stress disorder (PTSD) with a mixture of anxiety. The idea that flashbacks resulted from the changes in the brain has been outweighed due to the observation that cocaine due to a different mechanism of action causes flashbacks. There are a large number of people that have never taken any illicit drugs but they are suffering from severe anxiety and flashbacks. Their condition is due to some psychological problem. It can be concluded that flashbacks do not results form the damage of brain (Gawin & Kleber 1986).
Disturbed Sleep People suffer from insomnia after taking cocaine that continues for several days but it is also found that it may persist for several months in which the sufferers undergo excessive dreaming and they dream nightmares too (Reynolds & Kupfer 1987). Treatment Many drugs originally designed for other purposes may be helpful in treating cocaine addiction. Is one experiment, mecamylamine, which blocks the action of nicotine and may help smokers to quit, was given to crack cocaine users who also smoked tobacco cigarettes (as the vast majority does).
When exposed to a cocaine-related cue, they showed less intense craving than controls that had been given a placebo. Selegiline, an antidepressant that blocks the action of an enzyme that breaks down dopamine, has been tested as a treatment for cocaine addicts. Other related antidepressants (called MAO-B inhibitors) may help to control mood changes that occur during cocaine withdrawal. Several studies have found that Antabuse (disulfiram), which provokes nausea when taken with alcohol, also reduces the effect of cocaine in addicts.
But the prospects for these drug treatments are still in doubt. The effect of cocaine is difficult to neutralize, because anything that blocks its action is likely to block the dopamine transporter itself as well. Besides, addicts often lack the will to continue taking a prescribed drug every day. So scientists are now looking for ways to prevent cocaine from reaching the brain in the first place. They are trying to provide immunity against cocaine euphoria by targeting the drug in the bloodstream as if it were an infectious agent — a virus or bacterium.
But the body doesn’t normally attack cocaine as an invader, because the drug molecule is too small to be detected by the immune system or breaks down too quickly to elicit an antibody response. To overcome this obstacle, scientists at the Scripps Research Institute in La Jolla have created a stabler version of cocaine and linked it to a large carrier protein. The immune system can recognize the cocaine-protein complex as a foreign substance and produce antibodies, which will then attack cocaine itself.
The Scripps researchers reported that vaccinated rats given cocaine injections had up to 77% less in their brains than controls and were less likely to show the stereotyped body movements (e. g. , rearing and sniffing) usually induced by the drug (General Accounting Once 1997). In contrast with this active immunization (stimulating the human immune system to manufacture its own antibodies), a few researchers are considering the possibility of passive immunization — developing and cloning cocaine-specific antibodies in laboratory animals and modifying them so that they will not be attacked by the human immune system.
Fully human antibodies are now being produced in transgenic mice. A serious deficiency of these techniques is that each antibody combines permanently with one cocaine molecule; an addict can overwhelm the defense by taking a higher dose of cocaine. To overcome this limitation, another technique has been developed at Columbia University — the use of catalytic antibodies that would function as enzymes, breaking up one cocaine molecule into harmless substances and emerging intact to take on others.
Catalytic antibodies are at the animal testing stage right now, and many technical difficulties remain before this form of immunization can work fast enough to destroy cocaine molecules before they cross the blood-brain barrier. Immunization has several theoretical advantages over drug treatments. Because it does not occupy receptors in the brain, it does not cause side effects either in dopamine pathways or in brain regions using related neurotransmitters.
Attacking cocaine at a preliminary stage may also prevent such toxic effects as reduced brain blood flow. The ability to break cocaine’s reward cycle with antibodies could be enormously helpful for addicts who are genuinely committed to quitting. Even if some cocaine slipped past the guards and reached the brain, the resulting euphoria would not be as intense as usual and the craving might not be as great. And the value of a vaccine does not depend on the willingness of addicts, who are notoriously unreliable, to take a prescribed drug consistently.
Vaccines remain effective for weeks to months, and potentially even longer with booster shots (Higgins et al. 1993). Addiction is a complex illness, and there are no easy cures. Drug therapy or immunization alone will probably be no more effective than behavior therapy or psychotherapy alone. As long as patients still have a predisposition that leads to addiction, they may relapse or replace cocaine with another drug of abuse (almost all cocaine addicts also abuse alcohol and other drugs).
At best, by reducing craving and the temptation to relapse during the critical early period of abstinence, new and prospective medical treatments will provide time for psychological and social therapies to take effect. The neurochemical sources of cocaine’s attraction are still not completely understood. The medial forebrain bundle and other brain regions contain many kinds of receptors for dopamine with different functions, and it is not clear which ones are most responsible for the addiction. Nor is dopamine the only neurotransmitter involved.
According to recent research, even mice bred to lack the dopamine transporter molecule will inject cocaine, possibly because their brains have adapted to the loss or because there is a parallel reward system that goes into action when the primary one fails. One candidate for a transmitter in that system is serotonin, another chemical messenger whose reabsorption is blocked by cocaine (Carroll et al. 1994). Still other brain circuits and neurotransmitters may be involved in the conditioned learning that creates the risk of relapse in response to cues and associations.
This learning is probably governed by the prefrontal cortex and amygdala, which light up on brain scans when an addict is presented with a cocaine-related cue. Researchers are trying to sort out the complex interactions among brain regions and neurotransmitter systems that underlie cocaine addiction. They are also looking for hereditary roots of individual differences in susceptibility, which may lie in genes that govern the manufacture of receptors for dopamine and other transmitters. Conclusion Cocaine addiction leads to several psychiatric disorders. Emphasis should be made on providing the appropriate treatment.